The hepatic low-density lipoprotein receptor （LDLR） pathway is essential for clearing circulating LDL and is an important therapeutic target for treating cardiovascular disease. Abundance of the LDLR is subject to both transcriptional and non-transcriptional control. Here，we highlight a new post-transcriptional mechanism for controlling LDLR function via ubiquitination of the receptor by the inducible degrader of the LDLR （Idol）. Idol is a recently identified transcriptional target of the liver X receptors （LXR），acting as an E3-ubiquitin ligase. Idol promotes ubiquitination of the LDLR，thereby marking it for lysosomal degradation. Idol also targets two related lipoprotein receptors，the very low-density lipoprotein receptor and apolipoprotein E receptor 2. Despite several similarities，the Idol and PCSK9 pathways for controlling LDLR abundance seem independent of each other. Recent work has also suggested links between Idol and human LDL levels，thereby highlighting the possible role of Idol in human lipoprotein metabolism.